The bile-gut axis and metabolic consequences of cholecystectomy
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The bile-gut axis and metabolic consequences of cholecystectomy. / Lange, Andreas H.; Pedersen, Miriam G.; Ellegaard, Anne Marie; Nerild, Henriette H.; Brønden, Andreas; Sonne, David P.; Knop, Filip K.
In: European Journal of Endocrinology, Vol. 190, No. 4, 2024, p. R1-R9.Research output: Contribution to journal › Review › Research › peer-review
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TY - JOUR
T1 - The bile-gut axis and metabolic consequences of cholecystectomy
AU - Lange, Andreas H.
AU - Pedersen, Miriam G.
AU - Ellegaard, Anne Marie
AU - Nerild, Henriette H.
AU - Brønden, Andreas
AU - Sonne, David P.
AU - Knop, Filip K.
N1 - Publisher Copyright: © The Author(s) 2024. Published by Oxford University Press on behalf of European Society of Endocrinology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact
PY - 2024
Y1 - 2024
N2 - Cholelithiasis and cholecystitis affect individuals of all ages and are often treated by surgical removal of the gallbladder (cholecystectomy), which is considered a safe, low-risk procedure. Nevertheless, recent findings show that bile and its regulated storage and excretion may have important metabolic effects and that cholecystectomy is associated with several metabolic diseases postoperatively. Bile acids have long been known as emulsifiers essential to the assimilation of lipids and absorption of lipid-soluble vitamins, but more recently, they have also been reported to act as metabolic signaling agents. The nuclear receptor, farnesoid X receptor (FXR), and the G protein-coupled membrane receptor, Takeda G protein-coupled receptor 5 (TGR5), are specific to bile acids. Through activation of these receptors, bile acids control numerous metabolic functions. Cholecystectomy affects the storage and excretion of bile acids, which in turn may influence the activation of FXR and TGR5 and their effects on metabolism including processes leading to metabolic conditions such as metabolic dysfunction-associated steatotic liver disease and metabolic syndrome. Here, with the aim of elucidating mechanisms behind cholecystectomy-associated dysmetabolism, we review studies potentially linking cholecystectomy and bile acid-mediated metabolic effects and discuss possible pathophysiological mechanisms behind cholecystectomy-associated dysmetabolism.
AB - Cholelithiasis and cholecystitis affect individuals of all ages and are often treated by surgical removal of the gallbladder (cholecystectomy), which is considered a safe, low-risk procedure. Nevertheless, recent findings show that bile and its regulated storage and excretion may have important metabolic effects and that cholecystectomy is associated with several metabolic diseases postoperatively. Bile acids have long been known as emulsifiers essential to the assimilation of lipids and absorption of lipid-soluble vitamins, but more recently, they have also been reported to act as metabolic signaling agents. The nuclear receptor, farnesoid X receptor (FXR), and the G protein-coupled membrane receptor, Takeda G protein-coupled receptor 5 (TGR5), are specific to bile acids. Through activation of these receptors, bile acids control numerous metabolic functions. Cholecystectomy affects the storage and excretion of bile acids, which in turn may influence the activation of FXR and TGR5 and their effects on metabolism including processes leading to metabolic conditions such as metabolic dysfunction-associated steatotic liver disease and metabolic syndrome. Here, with the aim of elucidating mechanisms behind cholecystectomy-associated dysmetabolism, we review studies potentially linking cholecystectomy and bile acid-mediated metabolic effects and discuss possible pathophysiological mechanisms behind cholecystectomy-associated dysmetabolism.
KW - bile acids
KW - cholecystectomy
KW - GLP-1
KW - MASLD
KW - metabolism
U2 - 10.1093/ejendo/lvae034
DO - 10.1093/ejendo/lvae034
M3 - Review
C2 - 38551177
AN - SCOPUS:85190399486
VL - 190
SP - R1-R9
JO - European Journal of Endocrinology
JF - European Journal of Endocrinology
SN - 0804-4643
IS - 4
ER -
ID: 389458930